Hepatic encephalopathy is a fatal complication of both chronic liver disease and acute hepatocellular failure. Usually, in such cases, the disease has a rapid progression and fatal prognosis. We report a young female who was admitted in Medical College, Kolkata, India, in 2016 with clinical and biochemical evidence of encephalopathy and coagulopathy (hyperacute liver failure) following an acute hepatitis-like illness. Blood for hepatitis B surface antigen, anti-hepatitis C virus, IgM-hepatitis A virus, and IgM anti-Leptospira all were negative, but anti-hepatitis E virus (HEV) IgM came out to be positive (titer of 6.8 U/ml; whereas <0.9 – negative, 0.9–1.1 – borderline, and >1.1 – positive). IgM anti-HEV was tested using commercially available ELISA kits (Genelabs) using sandwich ELISA technique. The patient was aggressively managed with intravenous fluid, antibiotics, lactulose syrup and enema, and transfusion of fresh frozen plasma along with strict monitoring for other vital organ damage. Symptoms of encephalopathy completely reversed within 5–6 days, and prothrombin time and liver enzymes were normalized gradually. Although acute liver failure with high mortality is common in acute hepatitis E in pregnancy, here, in our case, it happened to a young nonpregnant female followed by complete recovery.

Keywords:Encephalopathy, hepatitis E, prothrombin time

How to cite this article:Chandra A, Sen I. A case of hepatic encephalopathy in an young female due to acute hepatitis E followed by complete recovery: A rare case report. Med J DY Patil Vidyapeeth 2018;11:539-41

How to cite this URL:Chandra A, Sen I. A case of hepatic encephalopathy in an young female due to acute hepatitis E followed by complete recovery: A rare case report. Med J DY Patil Vidyapeeth [serial online] 2018 [cited 2018 Dec 19];11:539-41. Available from: http://www.mjdrdypv.org/text.asp?2018/11/6/539/245419

Introduction

Infection with hepatitis E usually causes acute hepatitis along with self-limiting clinical course.[1],[2] Although the chances of acute liver failure with high mortality are relatively common in pregnant females, it is relatively rare in nonpregnant immunocompetent young individuals.[3],[4],[5]

Case Report

A 24-year-old female patient, homemaker, presented to us with chief complaints of yellowish discoloration of eyes and urine for the past 5 days followed by disorientation and irrelevant talks with alteration of sleep rhythm for 2 days. Prodromal symptoms in the form of anorexia and vomiting were present for 1 week before the onset of jaundice.

The patient was not known diabetic/hypertensive. There was no history of burning micturition, rash burning micturition, rash, or bleeding manifestation, nor any history of pain abdomen, itching, or passage of clay-colored stool. There was also no history of pedal swelling/puffiness of the face. There was no history of hematemesis and melena or history of blood transfusion. There was no significant drug history. There was no history of similar/any major illness in the past. There was no history of similar/any major illness in his family.

On personal history, she had no addiction and no history of multiple unprotected sexual intercourses. Her sleep cycle was altered and appetite was decreased.

On examination, the patient was disoriented about time, place, and person. However, there was marked icterus. Constructional apraxia and flapping tremor were present. Clubbing/pallor/cyanosis was absent, pulse was 100/m, and regular blood pressure was 100/70 mmHg. No significant skin/hair/nail changes were found. Jugular venous pulse was not elevated. No significant lymphadenopathy was detected. There was no hepatosplenomegaly or shifting dullness. Other systemic examinations were also within normal limit. On routine investigations, hemoglobin was 11.5 g/dl, total leukocyte count – 9,600/dl, platelet – 1.7 lakhs/dl, and on differential count, neutrophil was 65/lymphocyte was 23/monocyte was 6/eosinophil was 6. Erythrocyte sedimentation rate was 50 mm in the 1st h and mean corpuscular volume/mean corpuscular hemoglobin (MCH)/MCH concentration was 81.5/25.4/31.2, respectively. Urea and creatinine were 15 mg/dl and 0.7 mg/dl. Uric acid was 7.1 mg/dl. Serum sodium was 136 mEq/L and potassium was 4.4 mEq/L. Liver function test revealed that total bilirubin was 15.8 mg/dl, direct bilirubin was 11.0 mg/dl, aspartate transaminase was 314 U/L, alanine transaminase was 1408 U/L, and alkaline phosphatase was 324 U/L. Total serum protein was 6.3 g/dl along with albumin:globulin ratio of 1.1:1. Urine for routine examination revealed that pus cells were nil and pH was 7.0 with no cast or crystals. Prothrombin time was 48.80 (control 10.8 with INR 4.13) which prompted us for fresh frozen plasma transfusion. We searched for the cause of jaundice with hyperacute liver failure that revealed hepatitis B surface antigen, anti-hepatitis C virus, IgM-hepatitis A virus, and IgM anti-Leptospira all were negative, but anti-hepatitis E virus (HEV) IgM came out to be positive (titer of 6.8 U/ml; whereas <0.9 – negative, 0.9–1.1 – borderline, and >1.1 – positive). IgM anti-HEV was tested using commercially available ELISA kits (Genelabs) using sandwich ELISA technique. As hyperacute liver failure is not an uncommon presentation of acute hepatitis E with pregnancy, we did urine for pregnancy test. Urine for pregnancy test was negative. Blood for HIV1 and HIV2 was negative. Ultrasonography whole abdomen was done and reported as normal. The patient party was counseled for transferring the patient to a liver transplant unit, but they could not. At first intravenous fluid (dextrose containing) along with injection cefotaxime, lactulose syrup and enema were started. Then, she was given fresh frozen plasma for 2–3 days as there was significant prolongation of prothrombin time. The patient responded to these and his clinical condition was improving. All features of encephalopathy completely reversed within 5 days.

During our ward rounds, all features of encephalopathy completely reversed within 5 days. Subsequently, prothrombin time gradually normalized with INR of 1.79 after 3 days and 1.51 after 7 days. Liver function test repeated after 5 days showed significant improvement. The patient improved significantly with time, prothrombin time gradually normalized, bilirubin and liver enzymes gradually decreased, and the patient was discharged in a clinically and hemodynamically stable condition after 10 days.

Discussion

Hepatitis E is an enterically transmitted infection that is typically self-limited.[1] It is caused by Hepatitis E virus and spread by fecally contaminated water within endemic areas.[2] The course of infection has two phases – prodromal and icteric phase. Although most patients recover, mortality rate is high among pregnant females and patients with underlying chronic liver disease.[6] Severe acute liver injury was defined as a sudden deterioration in liver function confirmed by liver function tests and coagulopathy or presence of hepatic encephalopathy.[7] In patients with acute severe liver injury, HEV testing should be part of initial algorithm irrespective of age or initial suspicion.[3] The patient in the current case had developed acute liver failure following acute hepatitis E. Acute nontravel-associated hepatitis E can appear as fulminant hepatitis with features of coagulopathy and encephalopathy. Prognosis is severe and depends on age or preexisting liver disease.[4] HEV-infected pregnant women have a higher rate of fulminant hepatic failure and higher mortality rate in comparison to those nonpregnant women. Acute HEV infection is severe in the 2nd and 3rd trimester of pregnancy. It may lead to fulminant hepatic failure and death in 30%–100% of patients.[8] There is significantly higher occurrence of hepatitis E infection, chance of progression to encephalopathy, and higher mortality rates in pregnant women than nonpregnant.[5],[9] Treatment in such a condition is mainly symptomatic, some requires liver transplantation, although a report showed significant improvement of liver enzymes and function in a patient with severe acute hepatitis E who was treated with ribavirin for 21 days.[10] In our case, as the patient could not be transferred to a liver transplant center, she was managed symptomatically with dextrose-containing intravenous fluid to prevent hypoglycemia, antibiotics for high susceptibility to infections, lactulose syrup and enema, and transfusion of fresh frozen plasma to correct coagulopathy along with strict monitoring of other vital organ damage in a critical care unit.

Although acute infection with hepatitis E is usually self-limiting in nonpregnant individuals, it may be associated with fulminant liver failure as in our case. Our patient also recovered completely with conservative management although fulminant liver failure is associated with high mortality.

Declaration of patient consent

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